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目的考察紫贻贝金属硫蛋白(metallothionein,MT)对小鼠体内Cd~(2+)的拮抗及排除功效。方法采用0.5 mg/L CdCl_2饲喂小鼠,建立Cd~(2+)染毒小鼠模型;设立正常对照、CdCl_2模型、MT(50、75、100 mg/(kg·d))和依地酸二钠钙(75 mg/(kg·d))组,连续给药3 d、停止4 d,持续30 d后,分析小鼠生理指标、Cd~(2+)含量、抗氧化能力及肠道菌群组成。结果与正常组相比,模型小鼠体重、肝脏和脾脏重量及其系数显著降低(P<0.05),依地酸二钠钙和较高剂量MT给药,表现出显著改善小鼠生理指标作用。模型小鼠全血、肝脏及骨中Cd~(2+)含量显著增加(P<0.05),依地酸二钠和MT给药对体内Cd~(2+)排除显著(P<0.05)。相比正常组和模型组,MT对小鼠体内总抗氧化能力(total antioxidant capacity,T-AOC)和丙二醛(malondialdehyde,MDA)含量具有显著改善作用(P<0.05)。与正常组相比,Cd~(2+)染毒显著影响小鼠肠道正常菌群关系,造成菌群丰度和多样性减少;而MT对染毒小鼠肠道菌群结构、微生物多样性及丰度,均具有一定恢复作用。结论 MT具有拮抗Cd~(2+)体内富集及排出功效,其机制可能通过修复Cd~(2+)氧化损伤、减少过氧化产物水平及调节肠道菌群结构等途径实现。
Objective To investigate the antagonism and exclusion effect of metallothionein (MT) on Cd2 + in mice. Methods Cd 2+ mice were fed with 0.5 mg / L CdCl 2 to establish Cd 2+ -induced mice model. The normal control, CdCl 2 model, MT (50,75,100 mg / (kg · d)), After being dosed for 3 days and stopped for 4 days, the mice were sacrificed for 30 days. The physiological indexes, Cd2 + content, antioxidant capacity and intestine Road flora. Results Compared with the normal group, the body weight, liver and spleen weights and their coefficients of model mice were significantly decreased (P <0.05), calcium edetate disodium and higher dose of MT showed significant effects on the physiological indexes of mice . The content of Cd2 + in whole blood, liver and bone of model mice increased significantly (P <0.05). Disodium edetate and MT administration significantly (P <0.05) eliminated Cd2 + in vivo. Compared with the normal group and the model group, MT had a significant improvement on total antioxidant capacity (T-AOC) and malondialdehyde (MDA) in mice (P <0.05). Compared with the normal group, Cd ~ (2+) exposure significantly affected the normal intestinal microflora in mice, resulting in a decrease in the abundance and diversity of the bacteria. However, the activity of MT in the intestinal microflora, microbial diversity Sex and abundance, all have a certain role in recovery. CONCLUSION: MT can antagonize Cd2 + accumulation and efflux in vivo, and its mechanism may be through the repair of oxidative damage of Cd2 +, reduction of the level of peroxidation product and regulation of intestinal flora structure.